"Gene editing to remove viruses brings transplant organs from pigs a step closer," The Guardian reports after researchers used the new CRIPSR gene editing technique. CRIPSR acts like a set of molecular scissors that can cut out potentially harmful infectious genes.

Despite the difference in size and shape, many of the pig's internal organs are remarkably similar to human organs, making them a candidate for organ donations. The drawback is that some pigs carry what are known as porcine endogenous retroviruses (PERVs).

Retroviruses are a group of viruses that can cause various cancers and immunodeficiency illnesses, including HIV, which affect people. This has been found to make any attempt to use "unedited" pig cells for donation unsafe.

The researchers showed they could use CRIPSR to target the areas of the pig DNA that carried the retroviral code. Using this technique they were able to successfully remove all retroviruses from the pig cells.

These gene-edited cells were used to create pig embryos, which were implanted into surrogate sows. The resulting piglets were free from PERVs.

This research is a promising step forward in the possible use of pig organs to meet the massive shortage of human organ donors. However, there are many more stages of research to go and there are likely to be other practical, ethical and safety issues to overcome before using pigs as organ donors.

Until further progress is made you can help by signing up to the NHS Organ Donation register. You can sign up online, it takes just a few minutes.

Where did the story come from?

The study was carried out by researchers from eGenesis Inc in the US, Zhejiang University, China, and other institutions in China, the US and Denmark. The study was mainly funded by eGenesis Inc. and the US National Institute of Health, with other funding grants awarded to individual researchers.

eGenesis Inc is a US biotech firm working on trying to make animal-to-human organ transplant safe and effective. This technique is known as xenotransplantation.

The UK media give balanced coverage of this research by making it clear there were a number of hurdles to be cleared before xenotransplantation could become a reality.

What kind of research was this?

This laboratory study aimed to see whether it was possible to remove porcine (pig) retroviruses, which can infect human cells, from genetically modified pigs.

Retroviruses are a group of viruses that carry their genetic material in ribonucleic acid (RNA) and are named because of the enzyme reverse transcriptase that transforms RNA into DNA. The retrovirus group can cause various cancers, neurodegenerative disorders and HIV.

Pigs show potential as organ donors for humans as their organs are similar in size and function and they can be bred in large numbers. Porcine retroviruses (PERVs) are currently one of the big safety barriers preventing us using pigs as organ donors.

What did the research involve?

The researchers first demonstrated that porcine retroviruses are transferred to human cells. They transferred pig epithelial cells (which line organs and other surfaces in the body) to human embryonic kidney cells. When the human embryonic cells (cells derived from embryos developed from eggs fertilised in the lab) were monitored for four months, the number of porcine retroviruses increased over time. They showed that these viruses had integrated into the human DNA and could be transmitted to other human cells.

The researchers then showed they were able to inactivate all 62 copies of porcine retroviruses from the pig epithelial cells, which safely eliminated virus transmission to the human embryonic cells.

The focus of the current study was to demonstrate that they could achieve the same results and inactivate porcine retroviruses from pig foetal fibroblast (connective tissue) cells.

Firstly they mapped the 25 viruses present in the genetic code of these cells. They then used the technique of "CRISPR Guide RNA" which guides enzymes to cut the DNA at specific locations, effectively editing out the genes carrying the virus.

What were the basic results?

With some modifications to the CRISPR Guide RNA technique, the researchers were eventually able to completely edit out of all retroviruses from the pig fibroblast cells. They also confirmed that the technique did not lead to unwanted alterations elsewhere in the DNA.

They then used these gene-edited fibroblasts to create pig embryos (using a technique called somatic cell nuclear transfer, SCNT). After confirming the resulting embryos were completely free from retroviruses, they were then transferred to surrogate sows.

From about 200-330 embryos per sow transferred across to 17 sows, they produced 37 piglets, of which 15 remained alive up to four months. The piglets from successful pregnancies were confirmed to have no retroviruses in their DNA. They also confirmed there weren't any abnormal structural changes to these piglets.

The researchers are continuing to monitor the longer term effects in these animals.

How did the researchers interpret the results?

The researchers conclude that they have shown porcine retroviruses can be passed from pig to human cells in the laboratory, highlighting "the risk of cross-species viral transmission in the context of xenotransplantation."

To work towards eliminating this risk, they used a technique called CRISPR Guide RNA to produce pig embryos, foetuses and live pigs free from the retroviruses.

Conclusion

This promising research shows that it can be possible to use gene editing techniques to eliminate retroviruses from pigs, removing one of the potential barriers to using genetically modified pigs as organ donors for humans.

There are a few points to note. As the researchers say, though they have shown that pig retroviruses can be passed onto human cells in the laboratory, we don't know what the effects would be in real life. We don't know whether pig retroviruses would be transferred to humans and whether they could cause cancers or immunodeficiency illnesses, for example.

The research is at an early stage. The study has shown that they can produce retrovirus-free piglets but moving onto pig organ donation is another step. While some pig tissues have been in medical use for decades, such as pig heart valves and insulin, there are likely to be various practical, ethical and safety steps to overcome when it comes to transplanting whole large animal organs into humans.

A number of experts responded to the news – highlighting both the positives and negatives.

Prof Darren Griffin, Professor of Genetics, University of Kent, says: "This represents a significant step forward towards the possibility of making xenotransplantation a reality," while Prof Ian McConnell, Emeritus Professor of Veterinary Science, University of Cambridge, cautions: "[Organ transplant] is a huge unmet need of modern medicine. But the use of animal organs such as pig kidneys and hearts is not without serious ethical and biosecurity concerns."

"Deadly gene mutations removed from human embryos in landmark study," reports The Guardian. Researchers have used a gene-editing technique to repair faults in DNA that can cause the often-fatal heart condition, hypertrophic cardiomyopathy.

This inherited heart condition is caused by a genetic change (mutation) in one or more genes. Babies born with hypertrophic cardiomyopathy have diseased and stiff heart muscles, which can lead to sudden unexpected death in childhood and in young athletes; often because they don't realise they have the condition and so put their heart under strain when exercising.

In this latest study researchers used a technique called CRISPR-cas9 to target and then remove faulty genes. CRISPR-cas9 acts like a pair of molecular scissors, allowing scientists to cut out certain sections of DNA. The technique has attracted a great deal of excitement in the scientific community since it was released in 2014. But as yet, there have been no practical applications for human health.

The research is at an early stage and cannot legally be used as treatment to help families affected by hypertrophic cardiomyopathy. And none of the modified embryos were implanted in the womb.

While the technique showed a high degree of accuracy, it's unclear whether it is safe enough to be developed as a treatment. The sperm used in the study came from just one man with faulty genes, so the study needs to be repeated using cells from other people, to be sure the findings can be replicated.

Scientists say it is now important for society to start a discussion about the ethical and legal implications of the technology. It is currently against the law to implant genetically altered human embryos to create a pregnancy, although such embryos can be developed for research.

Where did the story come from?

The study was carried out by researchers from Oregon Health and Science University and the Salk Institute for Biological Studies in the US, the Institute for Basic Science and Seoul University in Korea, and BGI-Shenzen and BGI-Quingdao in China. It was funded by Oregon Health and Science University, the Institute for Basic Science, the G. Harold and Leila Y. Mathers Charitable Foundation, the Moxie Foundation and the Leona M. and Harry B. Helmsley Charitable Trust and the Shenzhen Municipal Government of China. The study was published in the peer-reviewed journal Nature.

The Guardian carried a clear and accurate report of the study. While the reports from ITV News, Sky News and The Independent were mostly accurate, they over-stated the current stage of research, with Sky News and ITV News saying it could eradicate "thousands of inherited conditions" and the Independent claiming it "opens the possibility for inherited diseases to be wiped out entirely." While this may be possible, we don't know whether other inherited diseases might be as easily targeted as this gene mutation.

Finally, the Daily Mail rolls out the arguably tired cliché of the technique leading to "designer babies", which seems irrelevant at this point. The CRISPR-cas9 technique is only in its infancy and (ethics aside) it's simply not possible to use genetic editing to select desirable characteristics – most of which are not the result of one single, identifiable gene. No reputable scientist would attempt such a procedure.

What kind of research was this?

This was a series of experiments carried out in laboratories, to test the effects of the CRISPR-Cas9 technique on human cells and embryos.

This type of scientific research helps us understand more about genes and how they can be changed by technology. It doesn't tell us what the effects would be if this was used as a treatment.

What did the research involve?

Researchers carried out a series of experiments on human cells, using the CRISPR-cas9 technique first on modified skin cells, then on very early embryos, and then on eggs at the point of fertilisation by sperm. They used genetic sequencing and analysis to assess the effects of these different experiments on cells and how they developed, up to five days.

They looked specifically to see what proportion of cells carrying faulty mutations could be repaired, whether the process caused other unwanted mutations, and whether the process repaired all, or just some of, the cells in an embryo.

They used skin cells (which were modified into stem cells) and sperm from one man, who carried the MYBPC3 mutation in his genome, and donor eggs from women without the genetic mutation. This is the mutation known to cause hypertrophic cardiomyopathy.

Normally in such cases, roughly half the embryos would have the mutation and half would not, as there's a 50-50 chance of the embryo inheriting the male or female version of the gene.

The CRISPR-cas9 technique can be used to select and delete specific genes from a strand of DNA. When this happens, usually the cut ends of the strand join together, but this causes problems so can't be used in the treatment of humans. The scientists created a genetic template of the healthy version of the gene, which they introduced at the same time as using CRISPR-cas9 to cut the mutated gene. They hoped the DNA would repair itself with a healthy version of the gene.

One important problem with changing genetic material is the development of "mosaic" embryos, where some of the cells have corrected genetic material and others have the original faulty gene. If this happened, doctors would not be able to tell whether or not an embryo was healthy.

The scientists needed to test all the cells in the embryos produced in the experiment, to see whether all cells had the corrected gene or whether the technique had resulted in a mixture.

They also did whole genome sequencing on some embryos, to test for unrelated genetic changes that might have been introduced accidentally during the process.

All embryos in the study were destroyed, in line with legislation about genetic research on embryos.

What were the basic results?

Researchers found that the technique worked on some of the stem cells and embryos, but worked best when used at the point of fertilisation of the egg. There were important differences between the way the repair worked on the stem cells and the egg.

Only 28% of the stem cells were affected by the CRISPR-cas9 technique. Of these, most repaired themselves by joining the ends together, and only 41% were repaired by using a corrected version of the gene.

67% of the embryos exposed to CRISPR-cas9 had only the correct version of the gene – higher than the 50% that would have been expected had the technique not been used. 33% of embryos had the mutated version of the gene, either in some or all of their cells.

Importantly, the embryos didn't seem to use the "template" injected into the zygote to carry out the repair, in the way the stem cells did. They used the female version of the healthy gene to carry out the repair, instead.

Of the embryos created using CRISPR-cas9 at the point of fertilisation, 72% had the correct version of the gene in all their cells, and 28% had the mutated version of the gene in all their cells. No embryos were mosaic – a mixture of cells with different genomes.

The researchers found no evidence of mutations induced by the technique, when they examined the cells in a variety of ways. However, they did find some evidence of gene deletions caused by DNA strands splicing (joining) themselves together without repairing the faulty gene.

How did the researchers interpret the results?

The researchers say they have demonstrated how human embryos "employ a different DNA damage repair system" to adult stem cells, which can be used to repair breaks in DNA made using the CRISPR-cas9 gene-editing technique.

They say that "targeted gene correction" could "potentially rescue a substantial portion of mutant human embryos", and increase the numbers available for transfer for couples using pre-implantation diagnosis during IVF treatment.

However, they caution that "despite remarkable targeting efficiency", CRISPR-cas9-treated embryos would not currently be suitable for transfer. "Genome editing approaches must be further optimised before clinical application" can be considered, they say.

Conclusion

Currently, genetically-inherited conditions like hypertrophic cardiomyopathy cannot be cured, only managed to reduce the risk of sudden cardiac death. For couples where one partner carries the mutated gene, the only option to avoid passing it onto their children is pre-implantation genetic diagnosis. This involves using IVF to create embryos, then testing a cell of the embryo to see whether it carries the healthy or mutated version of the gene. Embryos with healthy versions of the gene are then selected for implantation in the womb.

Problems arise if too few or none of the embryos have the correct version of the gene. The researchers suggest their technique could be used to increase the numbers of suitable embryos.

However, the research is still at an early stage and has not yet been shown to be safe or effective enough to be considered as a treatment.

The other major factor is ethics and the law. Some people worry that gene editing could lead to "designer babies," where couples use the tool to select attributes like hair colour, or even intelligence. At present, gene editing could not do this. Most of our characteristics, especially something as complex as intelligence, are not the result of one single, identifiable gene, so could not be selected in this way. And it's likely that, even if gene editing treatments became legally available, they would be restricted to medical conditions.

Designer babies aside, society needs to consider what is acceptable in terms of editing human genetic material in embryos. Some people think that this type of technique is "playing God" or is ethically unacceptable because it involves discarding embryos that carry faulty genes. Others think that it's rational to use the scientific techniques we have developed to eliminate causes of suffering, such as inherited diseases.

This research shows that the questions of how we want to legislate for this type of technique are becoming pressing. While the technology is not there yet, it is advancing quickly. This research shows just how close we are getting to making genetic editing of human embryos a reality.

"Scientists studying cancer stumble on 'breakthrough' in search for baldness cure," announces The Daily Telegraph, adding that not only does this mean "a cream or ointment may soon cure baldness or stop hair turning grey" but also it could one day ... explain why we age".

Sadly for those of us with grey, or no, hair on top, these claims are arguably premature.

Researchers were actually conducting a study in mice looking into a rare genetic condition called neurofibromatosis, which causes tumours to grow along the nerves, when they discovered the role a protein called KROX20 plays in hair colour.

The KROX20 protein is produced in specific cells within each individual hair follicle. This in turn switches on production of another protein called SCF. This SCF protein is needed to support the mature pigment (colour) producing cells in the hair follicle, and if it is not produced the mice lose their hair colour and become white. If the mice lack the KROX20-producing cells completely, they cannot produce any new hair and become bald.

While the basic biology of cells in different mammals is very similar, researchers are likely to want to perform tests on human cells in the laboratory to confirm the findings apply to humans.

This advance does not automatically mean that researchers are "on the cusp" of curing baldness or grey hair. The research is at an early stage, and it is not yet known whether the loss of hair colour is reversible and, if so, how it might be reversed.

Where did the story come from?

The study was carried out by researchers from the University of Texas and was funded through various grants from the National Institutes of Health.

The study was published in the peer-reviewed scientific journal Genes & Development.

While it's necessary to explain why a particular piece of research might be important, the predictions of what might happen as a result of this study are premature.

The University of Texas issued a press release about the study and it would appear that this formed the basis of the Telegraph's and the Daily Mail's coverage. Both describe the research in very similar terms to the wording in the press release.

It is the press release which suggests that "The research also could provide answers about why we age in general as hair graying and hair loss are among the first signs of aging".

It is certainly not possible to say at this stage whether these very specific hair-related processes are related more widely to ageing.

What kind of research was this?

This was animal research which has looked at the biology of hair greying and hair loss.

The researchers were actually investigating what seemed to be a completely different topic – neurofibromatosis – which causes benign tumours (neurofibromas) to develop in the covering (called the "sheath") of nerves.

However, they found that one strain of mice that they genetically engineered to study this condition actually developed grey fur early in life. Therefore they carried out more experiments to look at why this was, and what they could learn about hair greying.

This type of research is commonly used to get a very detailed understanding of the biological processes that go on in the body. When researchers have a better understanding of how such a process works it helps them to work out ways they might be able to stop them if required (for example if they normally lead to hair greying or loss) and help people when these processes go wrong.

However, results are very early stage and much more research is needed before any new treatments could be developed.

What did the research involve?

The researchers genetically engineered mice to stop producing a protein called SCF – Stem Cell Factor – in a specific group of cells which also produces a protein called KROX20. They found, to their surprise, that these mice lost all hair colour. This started when they were around 30 days old, and about nine months later the mice's hair was completely white.

The KROX20 protein was known to switch on certain genes during development, including those important in making the fatty coverings (sheaths) of nerves. It is also active in certain cells within the hair follicles. Once researchers discovered its effect on hair colour they did further experiments into what role these cells were playing in hair colouration.

For example, they looked at the levels of pigment (melanin) in the hair over time. They also investigated exactly what type of cells were producing KROX20, and where they were found in the hair follicle. The researchers also looked at what happened if they killed off the KROX20-producing cells at a key point in their hair production cycle.

What were the basic results?

The researchers found that the cells in the hair follicles which produced KROX20 would normally also produce SCF.

This SCF was found to be needed to maintain mature pigment-producing cells (melanocytes) in the hair follicle.

If the KROX20-producing cells did not also produce SCF, the mice's follicles lost mature melanocytes, and their coats lost their colour because no new pigment (melanin) was being deposited into the hair as it grew. This process started early on in the mice's lives – by the time these mice were 11 days old the amount of melanin in the hair was starting to decrease.

The researchers found that the KROX20-producing cells were developing from the same line of cells that produced keratinocytes – a type of cell commonly found in the outer layer of skin (epidermis).

These cells were found initially in only a restricted area of the hair follicle, but gradually they increased in numbers and also spread to other areas in the hair follicle. This included contributing to the formation of the hair shaft.

The researchers also found that if they killed off the KROX20-producing cells in the hair follicle, then the mice grew no new hair.

How did the researchers interpret the results?

The researchers concluded that they had identified a group of "progenitor [cell]s which regulate hair growth and pigmentation", in part by helping maintain pigment-producing cells (melanocytes).

Conclusion

The current study identified a group of cells in the hair follicles of mice which are important both in forming the hair shaft to allow hair growth, and also in maintaining hair colour.

So far this research has been in mice, but the basic biology of cells in mammals is very similar, so it seems likely that the findings would also apply to humans. Researchers are also likely to want to perform tests on human cells in the laboratory to confirm their findings.

The findings represent an advance in what is known about how hair grows and maintains its colour. However, this doesn't automatically mean the researchers are "on the cusp of developing a cream or ointment to cure baldness or stop hair turning grey" as suggested in the Mail.

The research is at an early stage, and the researchers themselves note that they still need to carry out studies to look at whether the loss of hair colour is reversible. Carrying out research takes time, and not every advance in understanding results in successful treatments.

"Smoking in pregnancy hurts your grandkids by 'increasing their risk of autism'," The Sun brashly reports.

Researchers looked at data spanning multiple generations and reported a link between girls with autism symptoms and having a maternal grandmother who smoked.

They looked at data from more than 14,000 children, which included autism-related behavioural traits, such as poor social communication skills, and whether or not their grandmother smoked in pregnancy.

The results give quite a confusing and mixed picture. Girls whose grandmothers had smoked in pregnancy had increased likelihood of certain traits such as poor social communication skills and repetitive behaviours.

However, this link was only found if the girl's own mother had not smoked in pregnancy. And there was no such link for grandsons, although there was an increased likelihood of grandsons being diagnosed with autism if their grandmother smoked.

The study failed to look at a plethora of other factors that could potentially play a role in autism spectrum disorders. These include parent and child diet, parental alcohol consumption, exercise, weight and genetic influences.

So it's wise to interpret these results with a healthy dose of scepticism – although it remains the case that you should never smoke during pregnancy. Doing so increases the risk of stillbirth, premature birth, and the risk of the child developing asthma in later life.

Where did the story come from?

The study was carried out by researchers from the University of Bristol and was funded by the UK Medical Research Council, the Wellcome Trust and the Escher Family Fund/Silicon Valley Community Foundation.

The UK media's reporting on the story was generally accurate; making it clear that the study looked at behavioural traits linked to autism and not autism diagnoses as such.

However, it was inaccurate to report that a girl would be "67 per cent more likely to suffer poor social communication skills and repetitive behaviours" if her grandmother smoked during pregnancy. This risk was only found for poor social communication skills.

And as is so often the case, the headlines were far less subtle or precise than the actual reporting, such as The Sun's "GENERATION MAIM Smoking in pregnancy hurts your GRANDKIDS".

What kind of research was this?

This was an analysis of data from a long running UK cohort study of children. Researchers wanted to explore whether a child would be at increased risk of autism if their mother or father had been exposed to their own mother's (the child's grandmother's) smoking during pregnancy.

Autism spectrum disorders (ASD) are long-term developmental conditions characterised by difficulties with communication and social interactions and often a preference for set patterns and routines.

The cause(s) of ASD are not established. Many experts think a combination of genetic and environmental factors may be involved.

This type of research can be informative as it makes use of a very large group of people and can ask multiple questions, including about smoking, and measure multiple health outcomes, including ASD traits.

However, lots of hereditary, environmental and lifestyle factors might contribute to risk of ASD. When the causes are unknown, it is difficult to take all these factors into account and prove that a single one – in this case a grandmother's smoking – causes ASD.

They also reported on whether the child's own mother smoked or not during pregnancy.

What were the basic results?

After adjusting for confounding variables, the results showed that maternal grandmother smoking in pregnancy was linked with ASD traits:

Social communication: Among maternal grandmothers who smoked in pregnancy, granddaughters were 67% more likely to have a high score (odds ratio (OR) 1.67, 95% confidence interval (CI) 1.25 to 2.25). This was only found when the girl's own mother did not smoke. There was no link for grandsons.

Repetitive behaviour: Among maternal grandmothers who smoked in pregnancy, granddaughters were 48% more likely to have a high score (OR 1.48, 95% CI 1.12 to 1.94). This was again only found when their own mother did not smoke, and not in grandsons.

No links were found for speech coherence and sociability temperament.

When combining all grandchildren whose maternal grandmother smoked, there was a 53% increased likelihood of them being diagnosed with autism (OR 1.53, 95% CI 1.06 to 2.20). However, this particular finding was only statistically significant for grandsons.

How did the researchers interpret the results?

The researchers conclude that they found "an association between maternal grandmother smoking in pregnancy and granddaughters having adverse scores in Social Communication and Repetitive Behaviour measures that are independently predictive of diagnosed autism. In line with this, we show an association with actual diagnosis of autism in her grandchildren. Paternal grandmothers smoking in pregnancy showed no associations."

Conclusion

This study aimed to see whether smoking in pregnancy is linked with some traits of ASD in the smoker's grandchildren.

Although this was based on a large cohort of children, the results give quite a confusing and inconclusive picture. To be frank, the study raised more questions than it answered.

Maternal grandmother smoking was linked with ASD traits only in girls (in whom ASD is less common in any case) – and then only if their own mother did not smoke. When looking at actual diagnosed cases of autism, the link was only found in boys.

The study had some important limitations to consider:

Most of the data was on behavioural traits, not actual diagnosed ASD, which cannot necessarily be directly linked with autism diagnoses.

The causes of ASD aren't known. Although the researchers attempted to adjust for some confounding variables, many other environmental and lifestyle factors could be having an influence.

ASD traits and autism diagnoses were only found when their own mother had not smoked in pregnancy – which indicates that it might not be smoke exposure that directly increases risk of ASD.

The results rely on reports from parents on their own parents, which may have been subject to recall bias if they could not remember all the facts. Some may not have known with certainty if their own parents had smoked during pregnancy.

Although it was a large sample, it was not very diverse with most grandparents assessed being of a white ethnic background. This may make findings less relevant to other ethnic backgrounds.

Overall, the mixed findings of this study do not provide any further answers to the causes of ASD.

What is known with certainly is that smoking in pregnancy increases the risk of stillbirth and premature birth, and later in the child's life sudden infant death syndrome and asthma.

"Most cancers are caused by random mistakes in the genetic code when cells divide out of the blue, new research shows," the Daily Mail reports.

But this is an oversimplification of research that looked at the role spontaneous random mutations play in the development of certain cancers.

It's well known that environmental and hereditary factors are the cause of many cancers.

This study looked at the influence of a third factor: random genetic mutations that occur by chance as the body's cells repeatedly divide.

Researchers analysed cancer registry data from 69 countries worldwide to estimate the proportion of cancers that could be down to chance. They estimated just over a third of cancers worldwide could be down to chance mutations.

Looking at data for 32 cancers in the Cancer Research UK (CRUK) database, this proportion leapt to two-thirds for reasons that are currently unclear.

But the research has two key limitations, both of which the researchers openly acknowledge. First, these figures are only estimates and may not be accurate.

And second, it would be a mistake to think cancers can only have one cause. A combination of all three factors – environmental, hereditary and luck – could all contribute towards a specific cancer risk.

Where did the story come from?

The study was carried out by three researchers from the Johns Hopkins University School of Medicine, the Johns Hopkins Bloomberg School of Public Health, and the Johns Hopkins Kimmel Cancer Center in the US.

Funding was provided by the John Templeton Foundation, the Virginia and D. K. Ludwig Fund for Cancer Research, the Lustgarten Foundation for Pancreatic Cancer Research, and the Sol Goldman Center for Pancreatic Cancer Research.

The lead author of the study has worked, or is currently working with, a number of biotech firms with a commercial interest in cancer genetics.

Both the Mail Online and The Sun failed to make it clear that there's no single risk factor for cancer.

A combination of family history, environmental factors, and just pure bad luck can all contribute towards your risk of developing a certain type of cancer.

What kind of research was this?

This analysis of cancer registry data aimed to look at the relationship between how many divisions stem cells (early-stage cells that can develop into many different types of cell) make and rates of cancer globally.

It's understood cancer is the result of the gradual build-up of gene mutations, resulting in greater numbers of abnormal cells. But the cause of these mutations is often uncertain.

It's thought some could be down to hereditary (genetic) factors and some are environmental, but the researchers explored a third factor: random chance mistakes made during normal DNA replication.

As cells divide, it's always possible that a mistake occurs when the "genetic alphabet" contained inside each cell is copied.

Previous studies suggested the chance of mistakes could come down to the repeated division of stem cells.

The researchers considered that, unlike cancers caused by hereditary or environmental factors, those caused by mistakes in stem cell division should be evenly distributed across human populations.

What did the research involve?

The researchers analysed 423 cancer registries in 69 countries available through the International Agency for Research on Cancer (IARC). This is said to give coverage of two-thirds of the global population, or 4.8 billion people.

The researchers looked at 17 different types of cancer that have stem cell data recorded in the IARC.

They analysed the relationship between the number of stem cell divisions made in a particular tissue and lifetime risk of cancer in that tissue.

They then estimated what fraction of cancers could be down to hereditary, environmental, and chance division factors.

What were the basic results?

In all the countries' data the researchers looked at, they found a significant relationship between the number of stem cell divisions in a tissue and cancer rates.

The median correlation figure from birth to age 85+ was 0.80 (95% confidence interval [CI]: 0.67 to 0.84), which indicates a very strong relationship between the two (a figure of 1.0 would be an exact correlation).

The links were generally consistent across countries, though higher in European, North American and Oceania countries (correlation 0.81 to 0.83) than Asian, African and Latin American countries (0.72 to 0.73). The bigger age range covered also gave a stronger correlation.

The researchers estimated that if environmental influences could be theoretically reduced to zero, around 35% (95% CI: 30 to 40%) of the mutations behind cancer would still be down to chance.

They then looked at 32 specific types of cancer reported in the CRUK database and estimated, overall, 29% of cancer mutations were down to environmental exposures, 5% to genetics, and 66% down to chance.

However, the proportions varied considerably by type of cancer. CRUK estimated 42% of these cancers could be preventable.

How did the researchers interpret the results?

The researchers say their findings are consistent with previous observational studies, which have indicated the proportion of cancers that may be down to environmental factors.

They say the results "accentuate the importance of early detection and intervention to reduce deaths from the many cancers arising from unavoidable [chance] mutations."

Conclusion

The possibility that random gene mutations can occur when the body's cells repeatedly divide is obviously highly plausible and not really that revolutionary a theory.

However, these researchers have tried to quantify exactly what proportion of cancers could be down to chance. This brings us to the greatest limitation of this research: these are only estimates.

As the researchers themselves point out: "The actual contribution of [chance] mutations to any particular cancer type cannot be reliably estimated from such correlations."

The researchers estimated random chance could be behind just over a third of cancers worldwide. It's not immediately apparent why on the CRUK database this proportion suddenly leaps to two-thirds.

But we don't know that these figures are accurate, and they won't necessarily apply to any individual cancers.

The fact chance may be involved also doesn't take away the importance of modifiable risk factors in cancer development.

Though the CRUK database indicated two-thirds of 32 cancers could be down to chance, CRUK still estimate 42% of these cases could be prevented.

As the study's authors pointed out: "Primary prevention is the best way to reduce cancer deaths. Recognition of a third contributor to cancer – chance mutations – does not diminish the importance of primary prevention."

"Up to one in five women with breast cancer could benefit from a type of treatment currently only given to patients with a rare form of the disease," The Independent reports.

Research suggests around 20% of women with breast cancer may benefit from a new class of drug known as PARP inhibitors.

PARP (poly ADP ribose polymerase) inhibitors were designed to treat women with breast cancer related to inherited mutations in the BRCA1 and BRCA2 genes (the so-called "Angelina Jolie mutation", because of the film star's history of the mutation) which are thought to account for up to 5% of breast cancers.

But this latest research suggests that as many as one in five women with breast cancer could benefit from PARP inhibitors.

In the study, researchers designed a computer programme to recognise genetic "signatures" associated with problems in the body's ability to defend itself against cancer. These problems are linked to the BRCA1 and BRCA2 mutations.

The software looked for non-inherited genetic problems that were similar to the problems caused by inherited BRCA1 and BRCA2 mutations, which might mean they could be treated in the same way. Of the 560 people tested, the model found 90 people – around 20% of the group – had genetic problems similar to those caused by BRCA1 and BRCA2 mutations, suggesting they might also benefit from PARP inhibitors.

The next step would be to see whether using PARP inhibitors in these types of cases would be helpful.

Where did the story come from?

The study was carried out by researchers from more than 30 medical institutions, led by the Wellcome Trust Sanger Institute in the UK. It was funded by the European Community, the Wellcome Trust, Institut National du Cancer in France and the Ministry of Health and Welfare in Korea.

There are potential conflicts of interest as three of the researchers have a patent for the code and intellectual property rights of the algorithm used to identify BRCA1 and BRCA2 deficiency. Another researcher was involved in the invention of PARP inhibitors.

The Independent, The Sun and BBC News all gave accurate overviews of the research. However, reading the headlines, you would not realise that the drugs have not yet been tested in the groups that might benefit.

Also, The Independent's headline: "One in five breast cancer patients not receiving new treatment that could benefit them," suggests the drugs are being deliberately withheld, when in fact there had not previously been any suggestion they could help, and we still don't know whether they are helpful.

What kind of research was this?

This was laboratory research using whole genome analysis of tissue in the laboratory, and feeding it through computer algorithms. This sort of research is good at generating theories, but clinical trials are needed before we know the practical application of the results.

What did the research involve?

Researchers took DNA from breast cancer tumours removed from 560 people and did whole genome sequencing. They used DNA from people known to have inherited BRCA1 or BRCA2 mutations to develop a computer programme to recognise signature features linked to the mutations. The programme then compared these results with results from people with non-inherited breast cancer.

The programme created a model, called HRDetect, to spot people who didn't have the inherited BRCA1 or BRCA2 mutation, but did have DNA changes that made them deficient in BRCA proteins. HR refers to homologous recombination repair, a method by which BRCA1 and BRCA2 proteins defend cells against cancer.

They tested HRDetect on several groups, and looked to see if it could be used on biopsy samples, rather than large tissue samples from removed tumours. They tested it on ovarian and pancreatic cancers, as well as the initial breast cancer group.

What were the basic results?

The HRDetect model found that, in women with non-inherited breast cancer:

69 out of 538 breast tumours were BRCA1 or BRCA2 deficient

16 out of 73 ovarian cancer tumours were BRCA1 or BRCA2 deficient

5 out of 96 pancreatic cancer tumours were BRCA1 or BRCA2 deficient

The researchers say the model showed 98.7% sensitivity (meaning that it missed less than 2% of tumours which were BRCA1/BRCA2 deficient). This is very high. They don't report on specificity – how many might have been wrongly identified as deficient (also known as a false positive result).

The model performed as well on samples of tumours from small needle biopsies as on large specimens removed during surgery. This suggests that the model could be used early in the clinical process, from the patient's first biopsy. This might help direct treatment from an early stage.

How did the researchers interpret the results?

The researchers said the model was "extraordinarily effective" as a predictive tool.

"If the tumours with predicted BRCA1/BRCA2 deficiency also demonstrate sensitivity to PARP inhibitors, this would unearth a substantial cohort of patients who could be responsive to selective therapeutic agents," they add. They say that this is "potentially transformative" of treatment and recommend use of their model in trials of PARP inhibitors.

Conclusion

Advances in genetic technology are happening fast, improving our knowledge about which treatments may be most suitable for which types of cancer. However, testing these theories takes time, which can be frustrating for researchers, when newspaper headlines suggest people should already be receiving new treatments.

This study potentially widens the pool of people who may benefit from targeted cancer treatment with PARP inhibitors, from around 5% to around 20%. That's clearly good news, but the potential for benefit needs to be tested in clinical trials.

The researchers express a great deal of confidence in the accuracy of their model. It would still be useful to see it externally validated in other groups of people, before we can know how well it performs in the real world. It would also be useful to see how specific the test is, as well as how sensitive it is.

One question remains about the 20% figure. It's not clear how the researchers selected people to take part in the study. They deliberately selected 22 patients who were known to have BRCA mutations. But we don't know whether the others in the study were randomly selected and representative of all people with breast cancer. If they were not randomly selected, then the 20% figure may not hold true for the wider population of people with breast cancer.

"Redheads are more likely to develop Parkinson's," claims the Mail Online after a study found the gene that makes people with red hair susceptible to skin cancer also increases the risk of brain disease.

But the study didn't actually look directly at redheads (human ones, anyway). Instead, it used mice to look at whether a red hair gene called MC1R might be important in the region of the brain affected by Parkinson's. The study found the MC1R gene was active in this brain region in mice.

When researchers stopped the gene working, it led to nerve cells in this region dying, resulting in the mice developing progressive problems with movement.

The causes of Parkinson's disease in humans are not completely understood. While this research supports the possibility this gene plays a role, there are likely to be other genetic factors involved, as well as environmental factors.

Not all studies in humans have found a link between variants in the MC1R gene and Parkinson's. Even if there is some increase in risk associated with certain forms of this gene, it's likely to be relatively small.

Where did the story come from?

The study was carried out by researchers from Massachusetts General Hospital, Harvard Medical School and the University of California in the US, and the Tongji University School of Medicine in China.

The work was funded by the National Institute of Neurological Disorders and Stroke, the National Natural Science Foundation of China, the RJG Foundation, the Michael J Fox Foundation, the Milstein Medical Asian American Partnership Foundation, and the US Department of Defense.

The news headlines fail to capture the uncertainty about whether redheads are at greater risk of Parkinson's. Some studies have suggested this may be the case, but the evidence isn't conclusive.

The current research didn't look at this question directly – it looked at whether researchers could find a biological reason why there might be a link.

What kind of research was this?

This animal research looked at how a gene that determines whether people have red hair might also play a role in Parkinson's disease.

Other studies have suggested people with malignant melanoma – a skin cancer more common in redheads and fair-skinned people – might be at greater risk of Parkinson's. Studies have also shown higher than expected rates of melanoma in people with Parkinson's.

The researchers thought the link between the two conditions might be down to a gene called the melanocortin 1 receptor (MC1R) gene. People who carry certain versions of the MCR1 gene tend to have red hair and fair skin.

Some studies – but not all – have suggested carrying certain red hair MC1R variants and having red hair are also associated with an increased risk of Parkinson's disease.

The researchers wanted to look at whether the MC1R gene has an effect on nerve cells in the brain that produce a specific signalling chemical called dopamine.

In Parkinson's, these nerve cells die off, which causes the slow movement problems characteristic of the disease. If the gene is important in these cells, this would explain why there might be a link between red hair and Parkinson's.

Humans and other animals share many of their genes, so researchers often investigate what genes do in animals to give strong pointers of their roles in humans.

What did the research involve?

The researchers studied mice with a defective form of the MC1R gene. These mice have yellow coats, the equivalent of red hair in humans. The researchers compared these with normal mice with functioning MC1R genes.

They first looked at whether the MC1R gene in normal mice was active in the dopamine-producing nerve cells in the part of the brain affected by Parkinson's disease, the substantia nigra.

They compared the abnormal mice with the non-functioning MC1R gene and the normal mice to see whether the substantia nigra looked different and whether the mice moved differently. They also looked at how the defective gene might affect brain cells.

One way of producing mice with a Parkinson's-like condition is by exposing them to chemicals that kill the dopamine nerve cells.

The researchers looked at whether the abnormal mice were more susceptible to two different chemicals that can do this.

They then looked at whether "switching on" the protein made by the MC1R gene chemically might protect normal mice against the effects of one of these Parkinson's-inducing chemicals.

What were the basic results?

The researchers found the MC1R gene was normally active in the dopamine-producing nerve cells of the substantia nigra, which are typically affected by Parkinson's disease.

Mice with an inactive MC1R gene showed progressive problems with their movement. They moved around less in an open area compared with normal mice of a similar age, and the problem got worse as they aged.

These mice appeared to be losing dopamine-producing nerve cells in the substantia nigra.

Additional experiments suggested brain cells in these mice had more DNA damage from naturally occurring chemicals called free radicals.

The abnormal mice were more susceptible than normal mice to two different Parkinson's-inducing chemicals.

The researchers also found chemically activating the protein made by the MC1R gene in normal mice reduced the effects of these toxic chemicals.

How did the researchers interpret the results?

The researchers concluded that genetically "shutting off" MC1R signalling in mice leads to the death of some dopamine-producing nerve cells.

The researchers suggest this may mean drugs that target MC1R might help in Parkinson's. It also supports the possibility that the MC1R gene plays a role in the risk of both melanoma and Parkinson's disease.

Conclusion

This study looked at the role the red hair gene MC1R plays in the brains of mice. The findings suggest the gene has a part to play in keeping certain nerve cells in the brain alive.

The cells in question are those that die off in Parkinson's disease and cause the condition's characteristic movement problems.

These findings in mice are likely to need further investigation in human cells and tissue in lab studies.

Exactly what causes brain cells to die, causing Parkinson's disease, is unknown. As with many conditions, it's thought both genetic and environmental factors could play a role.

Research like this helps us gain a better understanding of the disease and how it might be treated or prevented.

But Parkinson's is a complex disease, and this new study has only looked at one small piece of a much bigger puzzle. For redheads, it may be comforting to know this link has not yet been proven beyond a doubt.

And not all studies in humans have found a link between variants in the MC1R gene and Parkinson's. In fact, a recent systematic review by some of the authors of this study looked into this.

The review gathered studies published to date that have investigated the link between red hair variants of the MC1R gene and Parkinson's disease.

Six studies assessing links with two variants of this gene were identified, but the studies couldn't quite exclude the possibility of no effect when pooled.

The review also identified two studies looking at hair colour. These studies found people with red hair were more likely to develop Parkinson's than people without red hair.

But these observational studies have several limitations – notably, they can't prove clear cause and effect because many other genetic, environmental and lifestyle factors could also be influencing any links seen.

And even if there is some increase in risk caused by this pigment gene, it's likely to be relatively small.

"Artificial human life could soon be grown from scratch in the lab, after scientists successfully created a mammal embryo using only stem cells," reports The Daily Telegraph. This is an extremely premature claim as it is based on a laboratory study using mouse stem cells. Stem cells are cells that have the potential to be transformed into specific and specialised cells, such as bone marrow or fat cells.

Rather than using a fertilised egg, researchers from Cambridge University artificially grew an embryo in a three-dimensional structure by combining two types of stem cells – those that would develop into an embryo and those that would normally develop into the placenta. They found that the arrangement of cell development was very similar to the development of a usual mouse embryo.

While the media described the possibility of artificially formed human life soon becoming a reality, this is very early-stage research. Aside from the strict regulations about embryo research, the technical challenges of developing artificially formed human life are immense.

Reports about artificially created "designer babies" remain the stuff of science fiction.

A more down-to-earth implication of this research is that it may help provide more information about the early stages of pregnancy, which could eventually lead to new fertility treatments.

Where did the story come from?

The study was carried out by researchers from the University of Cambridge and Akdeniz University, Turkey.

The study was funded by the Wellcome Trust and the European Research Council and was published in the peer-reviewed journal Science.

The UK media reporting of the story was generally accurate, describing the methods used by the researchers in this exploratory lab study.

The Guardian reported: "Artificial mouse cells grown from outside the body in a blob of gel shown to morph into primitive embryos, roughly equivalent to one third of way through pregnancy", making clear that this was a study carried out in mice and not humans.

What kind of research was this?

This was an experimental laboratory study in mice that aimed to mimic interactions in the development of an embryo by combining the early embryonic stem cells with the cells that form the placenta within a 3D scaffold to try to develop an artificial embryo. This scaffold is a gel that allowed the structure to grow in three dimensions

While these laboratory studies are good at discovering new biological processes and ways of mimicking them, it must be remembered that they are often – as in this case – very early-stage research that cannot yet be applied to humans. Laboratory research involving human embryos is strictly controlled and regulated.

What did the research involve?

The study looked at the development of mouse embryos combining embryonic stem cells and cells that form the placental tissue, rather than starting from a fertilised egg.

The researchers took mouse embryonic stem cells (ES cells) and trophoblast stem (TS) cells, which are cells that are used to develop the placenta in normal pregnancy, and put them in a scaffold in a gel culture that allowed them to develop together.

What were the basic results?

They found that as the cells multiplied, structures made from the ES and TS cells developed in the 3D scaffold.

Following the seven days, the TS cells, which will go on to become the placenta, grew in a separate section to the ES cells – which will form the embryo.

Of all the structures they created, 22% were made from both ES and TS cells, 61% from ES cells only and 17% from TS cells only.

The ES and TS cells developing together in a 3D scaffold arranged themselves into a structure very similar to a natural embryo.

The ES cells further split into two groups, one cluster called the mesoderm would normally go on to develop into the heart, bones and muscles. The other section would normally go on to develop into the brain, eyes and skin.

They found that the timing and spatial arrangement of the cell development was very similar to the development of a usual mouse embryo.

Conclusion

This early-stage research offers a good insight into the development of mouse embryos and the sequence of biological steps that take place up to the point of implantation in the womb and immediately afterwards. They could provide an insight into the early stages of human life.

However, this does not mean that the creation of artificial human life is now possible:

The study was carried out on mice stem cells, which have a very different biological make-up to humans so the processes may not be identical with human cells.

While the artificial mouse embryo seemed to behave like a natural one, it is unlikely it could develop to a healthy foetus, as other components – such as the yolk sac that provides nutrition – were missing.

Not all embryonic and trophoblast structures developed and the biological reason for this is not known.

Most importantly, experiments involving human embryos or embryonic tissues are strictly regulated in the UK. Current legislation prohibits the development of embryos beyond a limit of 14 days.

As Professor James Adjaye, Chair of Stem Cell Research and Regenerative Medicine at Heinrich Heine University says: "As always, these types of experiments using human stem cells are regulated but there is no 'universal regulatory body'. Each country has its own regulatory body, which will ultimately decide on whether human [embryonic and trophoblast stem cell] embryos can be generated and for how long they can be left in the petri dish to develop further. Of course, there should be an international dialogue on the regulation of such experiments."

It is reported that the research team behind this work now plans to carry out similar work using human cells – a move that is sure to attract more media controversy.

"Breast cancer drugs taken by thousands of women stop working because tumours 'outsmart' them," is the headline in The Sun.

Around 70% of breast cancer cases are what are known as oestrogen receptor-positive breast cancers. This means the cancerous cells use the hormone oestrogen as a type of "fuel" to help them reproduce and spread.

After surgery to remove the tumour, many women with this type of cancer are prescribed hormone treatments – tamoxifen or aromatase inhibitors – that cut off the supply of oestrogen to the cancer in the hope the tumour doesn't return.

But some women build resistance to the drugs, so researchers set out to understand why. They found a particular gene (CYP19A1) becomes amplified, where more copies of the gene are produced, in about one in five women (21.5%) treated with aromatase inhibitors.

This triggers the increased production of aromatase, the enzyme the drugs were trying to block. This enzyme converts hormones in the body into oestrogen. This allows the cancer cells to make their own oestrogen again, and reproduce and spread.

The researchers weren't able to understand the mechanism behind drug resistance to tamoxifen, but hope to carry out further research to find out how it occurs.

The team behind this study hope their work will pave the way for further research so they can develop a test able to identify whether a woman's tumour has already started to increase the production of aromatase. This may allow doctors to prescribe different and more effective forms of treatment.

Where did the story come from?

The study was carried out by researchers from several global institutions, including Imperial College London and the European Institute of Oncology in Milan.

Some of the researchers received support through grants from Cancer Research UK and the Associazione Italiana per la Ricerca sul Cancro. No conflicts of interest were reported.

The study was published in the peer-reviewed journal, Nature Genetics.

Although some of the headlines, such as The Mirror's, were slightly overoptimistic – "Breast cancer discovery could stop disease killing women and leave them with 'normal life expectancy'" – the UK media's reporting was generally well balanced.

However, this research more accurately applies to one in five women with oestrogen receptor-positive breast cancer treated with aromatase inhibitors – usually women who have gone through the menopause – not one in four women with breast cancer, as some headlines state.

What kind of research was this?

This laboratory study used human cell samples to investigate the mechanism behind how breast cancer tumours develop resistance to treatments, effectively making them powerless.

Approximately 70% of breast cancers are classified as oestrogen receptor-positive – where the cancer is fuelled by the hormone oestrogen.

In these cases, women can be offered one of two hormone treatments after surgery to prevent the cancer returning: tamoxifen or aromatase inhibitors.

Aromatase inhibitors are usually only given to women who've already been through the menopause, while tamoxifen may be given to pre- or postmenopausal women. The medication is designed to stop the production of oestrogen in the body or block its effects.

However, more than one in five women relapse within 10 years of this treatment, and eventually develop metastatic cancer that spreads to other parts of the body. This has spurred scientists on to explore the cause of tumour resistance.

Laboratory studies like this one are useful early-stage research for understanding complex biological mechanisms. They can pave the way for potential future treatment options, but are also able to identify gaps in research.

What did the research involve?

The researchers used samples of human breast cancer tumours from a database containing data on 26,495 women who had undergone surgery for first primary breast cancer between 1994 and 2014.

They had data available on the patients' medical history, concurrent disease, surgery, histology assessments, results of staging procedures, radiotherapy, treatments given after surgery, events occurring during follow-up, and treatments for recurrent metastatic disease.

This study analysed tumour samples from 150 women who had experienced a recurrence of breast cancer with metastatic spread to different parts of the body.

Fifty of the women only received aromatase inhibitors after surgery, and 50 only received tamoxifen.

The researchers used various genetic analysis methods to extract DNA and manipulate the hormones to learn more about the exact mechanism behind the resistance to treatment.

What were the basic results?

Overall, the researchers found the CYP19A1 gene became amplified and triggered the increased production of aromatase in about one in five women prescribed aromatase inhibitors after surgery.

Aromatase is the enzyme that normally converts circulating male hormones in the woman's body into oestrogen, which the aromatase inhibitors are trying to block.

The gene was essentially allowing the cancer cells to make their own supply of oestrogen hormone again, making the aromatase inhibitors ineffective.

The same mechanism doesn't seem to be behind tamoxifen resistance. In women taking tamoxifen, almost none of the tumours showed increased amplification of the CYP19A1 gene as seen in those taking aromatase inhibitors, so they weren't producing their own supply of oestrogen in this way.

The researchers hope to embark on further research to understand how cancer cells build resistance to tamoxifen, as this is clearly through a different mechanism.

How did the researchers interpret the results?

The researchers concluded that, "It is tempting to speculate that CYP19A1 amplification might arise in response to reversible inhibitors but could be antagonised [blocked] by switching to irreversible inhibitors.

"Alternatively, it should be clinically feasible to directly antagonise the low levels of circulating male hormones commonly found in postmenopausal women.

They go on to say that, "Taken together, our clinical data demonstrate that the evolution of breast cancer is shaped by clinical intervention and thus advocate the development of treatment and setting-specific biomarkers."

Conclusion

This laboratory study aimed to investigate the mechanism behind how some oestrogen receptor-positive breast cancer tumours develop resistance to the hormone drugs tamoxifen and aromatase inhibitors.

This resistance effectively makes these drugs powerless, causing the cancer to return.

The researchers seemed to find at least part of the answer as to why resistance to aromatase inhibitors can develop.

In some cases, they found treatment triggered the amplification of the CYP19A1 gene, which increased the production of aromatase, essentially allowing the cells to keep making their own oestrogen.

But this doesn't seem to tell us why drug resistance to tamoxifen develops. This seems to be the result of another mechanism and not related to the production of aromatase.

The researchers hope to investigate how resistance towards tamoxifen is established. They hope to further this research to work on developing a test that will be able to identify whether a woman's tumour has started to make its own supply of oestrogen through increased aromatase production.

One of the researchers, Dr Luca Magnani, commented: "In many cases when an aromatase inhibitor stops working in a patient, doctors will try another type of aromatase inhibitor.

"However, our research suggests that if the patient's cancer has started to make their own aromatase, this second drug would be useless. This is why we need a test to identify these patients."

The hope is that finding out more about why these drugs don't work for some women will lead to new drugs that do.

Where did the story come from?

The study was carried out by researchers from the University of California, San Diego State University, the State University of New York at Buffalo, the University of Washington, the Fred Hutchinson Cancer Research Centre, George Washington University, the University of Florida and Northwestern University, all in the US.

All of the UK media outlets that covered the study implied that a direct cause and effect relationship between sitting down and cell ageing had been proven.

For example, the Mail's headline stated that, "Women who spend at least 10 hours on their backsides each day speed up their aging process."

This is untrue. While there certainly seems to be an association worthy of further research, no causal link has been established.

What kind of research was this?

This cross-sectional study used data from women taking part in a much bigger study of health called the Women's Health Initiative.

Cross-sectional studies can find correlations between different factors – in this case, sitting time and telomere length.

But because this type of study only looks at one point in time, researchers can't say which factor happened first, so it's not very useful for telling us whether one causes the other.

What did the research involve?

Researchers used information about 1,481 women aged over 65 who'd taken part in various sub-studies of the Women's Health Initiative.

They used information from women who'd had their physical activity measured using accelerometers (devices that measure movement) and had also given DNA samples that had been tested for telomere length.

After accounting for other factors, they looked at whether telomere length was linked to the amount of time spent sitting.

The information about physical activity was measured over one week, during which time women wore their accelerometer all the time, except when bathing or swimming.

Women taking part also completed a questionnaire about their physical activity and kept a record of their sleep. Telomere length was measured from DNA in blood cells.

They also redid their calculations to divide the women into those who did more or less than the average amount of physical activity (about 40 minutes).

They then looked at the link between time spent sitting and telomere length for women who did more or less than 40 minutes physical activity a day.

They also looked at the link between sitting and telomere length for women who did 30 minutes or more a day, the recommended activity level for all adults.

It's unclear whether these additional calculations were planned from the start of the study, or whether the researchers decided to do them because the initial findings did not show a link between time spent sitting and telomere length.

What were the basic results?

The length of time spent sitting was not linked to telomere length for women who did 30 minutes or more of moderate physical exercise a day.

For women who did less than the average amount of moderate physical activity each day, time spent sitting did show a link to telomere length.

Among these women, those who spent more than about 10 hours a day sitting had shorter telomeres than those who spent less than about eight hours a day sitting. The average difference was 170 base pairs (95% confidence interval [CI] 4 to 340).

Women who spent the most time sitting were more likely to be older, white, obese and have long-term illnesses.

How did the researchers interpret the results?

The researchers said their results suggest that, "Prolonged sedentary time and limited engagement in moderate to vigorous physical activity may act synergistically to shorten leukocyte telomere length among older women."

In other words, being both sedentary for long periods and not getting much physical activity may act together to shorten telomeres in blood cells.

They speculated that causes of the link might include insulin resistance, lack of the anti-inflammatory responses the body has to exercise, or obesity.

They also acknowledged women who have long-term illnesses are more likely to have a sedentary lifestyle, and the illness rather than the lack of exercise may cause shortened telomeres.

Conclusion

It's not news to anyone that being more physically active and spending less time sitting around is likely to keep people in better health.

But this study has many limitations that make it difficult for us to rely on its results.

While they are used as a marker for ageing cells, telomeres are not a direct measure of ageing. Although shortened telomeres have been linked to certain diseases, everyone's telomeres shorten over time.

Saying shorter telomeres make someone "biologically older" doesn't mean much. This hasn't stopped the emergence of private companies offering to measure your telomeres – but it's unclear what exactly you could usefully do with that information.

And the only cells studied in this research were blood cells, so we don't know whether the results would have held for brain cells, muscle cells or any other cells in the body.

Doctors have tried to disentangle the effects of physical activity from the effects of being sedentary before without much success.

Generally, as in this study, research seems to show that if you get plenty of moderate to vigorous physical exercise, the amount of time you spend sitting or lying down doesn't make much difference.

The researchers carried out a lot of comparisons and used multiple models to try to show sedentary time was linked to telomere length.

In most of these models, once you take account of women's age, ethnicity, body mass index and long-term illnesses, there was no link.

Only when the researchers stratified the results by how much physical activity women did could they show a link in one category: those who did the least physical activity.

That suggests sedentary behaviour is not the strongest factor to affect telomere length.

Another problem with the study is it only looked at telomere length and physical activity at one point in the women's lives.

We don't know how much physical activity they'd done throughout their lives, or whether their telomeres had shortened faster than other women recently or at an earlier stage in life.